Meningitis
16-2-2015 mon zahraa
Meningitis is a disease caused by the inflammation of the protective
membranes covering the brain and spinal cord known as the meninges. The
inflammation is usually caused by an infection of the fluid surrounding the
brain and spinal cord.
Meningitis may develop in response to a number of causes, usually bacteria
or viruses, but meningitis can also be caused by physical injury, cancer or
certain drugs.
The severity of illness and the treatment for meningitis differ depending on
the cause. Thus, it is important to know the specific cause of meningitis.
Bacterial meningitis is usually severe. While most people with meningitis
recover, it can cause serious complications, such as brain damage, hearing
loss, or learning disabilities.
There are several pathogens that can cause bacterial meningitis. Some of the
leading causes of bacterial meningitis include Haemophilus influenzae (type
b, Hib), Streptococcus pneumoniae, group B Streptococcus, Listeria
monocytogenes, and Neisseria meningitidis.
Viral meningitis is the most common type of meningitis. It is often less
severe than bacterial meningitis, and most people usually get better on their
own (without treatment). However, infants younger than 1 month old and
people with weakened immune systems are more likely to have severe
illness.
enteroviruses
Mumps virus
Herpes viruses, including Epstein-Barr virus, herpes simplex viruses, and
varicella-zoster virus
Measles virus
Influenza virus
Fungal meningitis
is rare and usually the result of spread of a fungus through
blood to the spinal cord, people with weakened immune systems, like those
with HIV infection or cancer, are at higher risk.
The most common cause of fungal meningitis for people with weakened
immune systems is Cryptococcus.
Parasitic Meningitis
Non–infectious meningitis causes include
Cancers
Systemic lupus erythematosus (lupus)
Certain drugs, Head injury, Brain surgery
Meningococcal meningitis
Meningococcal meningitis is a bacterial form of meningitis, a serious
infection of the meninges that affects the brain membrane. It can cause
severe brain damage and is fatal in 50% of cases if untreated
Several different bacteria can cause meningitis. Neisseria meningitidis is
the one with the potential to cause large epidemics. Twelve serogroups of N.
meningitides have been identified, six of which (A, B, C, W135, X and Y)
can cause epidemics. Geographic distribution and epidemic potential differ
according to serogroup.
There are three clinical variants of the disease:
1. Nasopharyngitis alone: such cases are fairly common and account for
spread and occurrence of the disease in sporadic form. They show no
meningeal symptom and form the bulk of the missed meningococcal
infections. The infected person spread the disease through droplet
transmission.
2. Meningococcemia alone :characterized by acute septicemia and often a
petechial rash sometimes with joint involvements .
3. Cerebrospinal meningitis: this is the typical and most common form and
characterized by involvement of the meninges . Headache ,temp.(37.3_38.9),
slow pulse ,vomiting cervical rigidity ,kerning sign , Brudzinkis sign and in
young children opisthotonus are the common features.
Diagnosis
1. Demonstration of the of the typical organism in a gram stained smear of
the spinal fluid .
2. Culture of the organism from blood or CSF.
3. Latex agglutination (demonstration of meningococcal polysaccharide .
Occurrence
It occur in sporadic cases .
A large No. of healthy carrier s are found (50%)
Some cases get only nasopharyngitis, they spread the disease but remain
undetected.
Susceptibility to clinical disease is very low (high ratio of carriers to cases) .
Neisseria meningitidis only infects humans; there is no animal reservoir.
Causative agent
Neisseria meningitis or meningococcus (Neisseria meningitidis is a gram-
negative diplococcus. Meningococci are classified into serogroups on the
basis of the composition of the capsular polysaccharide. The 5 major
meningococcal serogroups associated with disease are A, B, C, Y, and W-
135.
Transmission
The bacteria are transmitted from person-to-person through
droplets of respiratory or throat secretions from carriers. Close and
prolonged contact – such as kissing, sneezing or coughing . living in close
quarters (such as a dormitory, sharing eating or drinking utensils) with an
infected person (a carrier) – facilitates the spread of the disease.
Source of infection
Carriers, patients, and mild cases of nasopharyngitis. The patient is infective
as long as the meningococci are present in oronasal discharge .
If the organisms are sensitive to sulphonamides , they disappear within 24
hours after treatment. Penicillin doesn’t eradicate them fully from
oropharynx. Children are more prone than adults. Mortality rate in
meningitis should be less than 10% if diagnosis is early and modern
therapeutic and support measure are used.
Incubation period
2-10 days, average 3-4 days.
Prevention and control
Isolation : this is needed up to 24 hours after the start of appropriate
chemotherapy.
Protection of contacts: Sulphadiazine for 5 days or Rifampicin for 2 days
given as a chemo prophylactic measure.
Treatment : Antibiotic of choice for treatment of meningitis is pencilin G.
Ampicillin used as alternative to pencillin. Chloramphenicol can be used
with precaution. Several types of vaccine are available: polysaccharide
vaccines — available in either bivalent (groups A and C), trivalent (groups
A, C and W135), or tetravalent (groups A, C, W135 and Y).
Get a meningococcal vaccine:
A dose of meningitis vaccine is recommended for people traveling to
countries in the “meningitis belt”
Travelers to the Hajj must show proof of vaccination in the past 3 years.
It takes approximately 7-10 days after receiving the vaccine before a person
can develop protection against the disease.
Nonspecific Viral Infections
Common Cold (Acute Coryza)
Among the acute respiratory illness two-thirds are caused by viruses. Most
of these viral infections affect the upper respiratory tract, but lower
respiratory tract can be involved in certain groups particularly in young age
group. The illness caused by respiratory viruses expressed into multiple
distinct syndromes, such as common cold, pharyngitis, croup,
tracheobronchitis, bronchiolitis, pneumonia.
Almost everybody suffers from common cold sometime in his life. It occurs
more in winter and in cold
Climates. It is an acute infection of the respiratory tract characterized by
sneezing, running nose, nasopharyngeal irritation and malaise lasting two to
seven days.
Fever is rare.
The infectious agent is a rhinovirus with more than 100 serotypes. The
patient is highly infective 24 hours preceding and five days following the
onset of the disease.
Transmission is by droplet or through fomites.
Susceptibility is general
Immunity is short lived and lasts for a month or so.
Incubation period is 12 to 72 (usually 24) hours.
There is no specific treatment.
vaccines have been used but the results are not encouraging.
Influenza
Influenza is an acute infectious respiratory disease caused by RNA viruses of
the family orthomyxoviridae (the influenza viruses). The influenza virus,
known to cause recurrent epidemics and global pandemics.
Genetic reassortments in the influenza virus cause fast and unpredictable
antigenic changes in important immune targets leading to recurrent
epidemics of febrile respiratory disease every one to three years. Each
century has seen some pandemics rapidly progressing to all parts of the
world due to emergence of a novel virus to which the overall population
holds no immunity
CLINICAL FEATURES
Infection with influenza may be asymptomatic but usually gives rise to fever
and typical prostrating disease, characteristic in epidemics. Usual symptoms
are flushed face, congested conjunctivae, cough, sore throat, fever for two to
three days, headache, myalgia, back pains and marked weakness. Pneumonia
due to secondary bacterial infection is the most common complication.
Laboratory confirmation is made by recovery of virus from throat washings
or by demonstration of significant rise of influenza antibodies in the serum
in acute and convalescent stages of the disease or by direct identification
of the virus in nasopharyngeal cells.
EPIDEMIOLOGY
A large number of cases are either missed or are unreported because of their
mildness. Morbidity rate varies from 15 to 25 percent of the population
exposed to risk in case of large communities. The rate may be as high as 40
percent in case of closed populations. Once an epidemic starts, its
peak is reached in three to four weeks before declining.
The disease was first recognized in 1173; since then
80 epidemics have occurred. The epidemic lasts for six to eight weeks at a
place. It is not known what happens to the virus between the epidemics.3
However,there is evidence that transmission of the virus to extra human
reservoirs (pigs, horses, birds, ducks) keeps the virus cycle alive.
antigenic drift less rapidly than influenza A viruses. Drift ensures an ongoing
turnover of viral strains and thus a constant renewal of susceptible hosts,
which is the basis for the regular occurrence of influenza epidemics.
Antigenic drift explains why a person can be infected by Influenza A viruses
several times and also why Influenza vaccine need to be updated every year.
Antigenic shift is the major antigenic change that results from genetic
reassortment between two different virus subtypes coinfecting the same cell
and developing a new subtype with completely new hemagglutinin and
neuraminidase antigen. Antigenic shift is noted only with type A influenza
virus. Antigenic shift appear to result from genetic reassortment between
human strains and avian or animal strains.
CHANGING NATURE OF VIRUS
New influenza virus strain may evolve due to point mutation or by genetic
reassortment. Two type of antigenic change may occur in the virus namely
antigenic drift and shift. Minor changes in the hemagglutinin and/or
neuraminidase antigens on the surface of the virus which results from point
mutation during viral replication is called antigenic drift. Antigenic drift
occurs in both Influenza A and B viruses. Influenza B viruses undergo
An example of antigenic shift
involving both the hemagglutinin and neuraminidase is that of 1957
influenza pandemic, when predominant sub type of influenza A shifted from
H1N1 to H2N2.The population has got no immunity against the newly
emerged strain, which can then spread to cause an ‘Influenza pandemic’.
Pandemics occur every 10 to 50 years. They have been documented since
the 16
th
century and in the last 400 years; at least 31 pandemics have been
recorded. During the twentieth century, three influenza pandemics occurred
CHARACTERISTICS OF INFLUENZA PANDEMICS
• Occurrence outside the usual season
• Extremely rapid transmission with concurrent
outbreaks throughout the globe
• High attack rates in all age groups with high mortality
rates even in young adults.
CAUSATIVE AGENT
Influenza viruses are RNA viruses of orthomyxoviridae family. The virus
has three distinct genera (types A, B or C) based on antigenic differences of
their nucleo and matrix proteins. Influenza A viruses are divided into
subtypes based on two proteins on the surface of the virus: the
hemagglutinin (H) and the neuraminidase (N).
Influenza B viruses are not categorized into subtypes. Currently among
many subtypes of viruses, influenza A (H1N1) viruses, influenza A (H3N2)
viruses, and influenza B viruses are circulating worldwide in human.
Epidemics are primarily caused by type A viruses and occasionally by type
B in human being. Type C influenza virus has been associated with sporadic
cases and minor localized outbreaks. Avian influenza viruses (AIV) belong
to type A influenza virus.
HOST FACTORS
Age and sex
: the influenza virus maximally attacks those in the age group 5
to 15 years but no age group or sex is spared. Rates of infection are highest
among children, but death and serious illness are common amongst persons
aged 65 years, children below two years and persons of any age with
associated medical conditions that place them at increased risk for
complications from influenza.
Immunity:
The antibody to H type of antigen prevents initiation of the infection while
that to N antigen prevents virus release and spread. The antibodies
developed in the respiratory tract following an infection are mostly IgA.
They appear in about seven days after an attack and peak in the blood by
two weeks. The level drops to pre infection level by 8 to 12 months.
Antibody against one influenza virus type or subtype confers limited or no
protection against another type or subtype of influenza. Furthermore
antibody to one antigenic variant of influenza virus might not completely
protect against a new antigenic variant of the same type or subtype. Frequent
development of antigenic variants through antigenic drift is the virologic
basis for seasonal epidemics and the reason for the usual
incorporation of one or more new strains in each year’s influenza vaccine.
MODE OF TRANSMISSION
Influenza viruses predominantly transmitted through respiratory droplets of
coughs and sneezes from an infected person. Influenza viruses may also
spread through direct (skin to skin) or indirect contact with infected material,
which ultimately enters through nasopharyngeal route. Transmission of
viruses starts one day before the onset of symptoms and continue up to five
to seven days after the symptoms subsides.
Transmission is possible from
asymptomatic carriers. Children may pass the virus for longer than seven
days. Influenza viruses can be inactivated by sunlight, disinfectants and
detergents easily. Frequent hand washing reduces the risk of infection.
DIAA